Crews Fulton T, Collins Michael A, Dlugos Cynthia, Littleton John, Wilkins Lincoln, Neafsey Edward J, Pentney Roberta, Snell Lawrence D, Tabakoff Boris, Zou Jian, Noronha Antonio
University at Buffalo, SUNY, NY, USA.
Alcohol Clin Exp Res. 2004 Feb;28(2):350-64. doi: 10.1097/01.alc.0000113416.65546.01.
This manuscript reviews the proceedings of a symposium organized by Drs. Antonio Noronha and Fulton Crews presented at the 2003 Research Society on Alcoholism meeting. The purpose of the symposium was to examine recent findings on when alcohol induced brain damage occurs, e.g., during intoxication and/or during alcohol withdrawal. Further studies investigate specific brain regions (where) and the mechanisms (why) of alcoholic neurodegeneration. The presentations were (1) Characterization of Synaptic Loss in Cerebella of Mature and Senescent Rats after Lengthy Chronic Ethanol Consumption, (2) Ethanol Withdrawal Both Causes Neurotoxicity and Inhibits Neuronal Recovery Processes in Rat Organotypic Hippocampal Cultures, (3) Binge Drinking-Induced Brain Damage: Genetic and Age Related Effects, (4) Binge Ethanol-Induced Brain Damage: Involvement of Edema, Arachidonic Acid and Tissue Necrosis Factor alpha (TNFalpha), and (5) Cyclic AMP Cascade, Stem Cells and Ethanol. Taken together these studies suggest that alcoholic neurodegeneration occurs through multiple mechanisms and in multiple brain regions both during intoxication and withdrawal.
本手稿回顾了由安东尼奥·诺罗尼亚博士和富尔顿·克鲁斯博士组织的一场研讨会的会议记录,该研讨会在2003年酒精研究学会会议上发表。该研讨会的目的是研究酒精性脑损伤何时发生的最新研究结果,例如在中毒期间和/或戒酒期间。进一步的研究调查了酒精性神经变性的特定脑区(何处)和机制(为何)。这些报告分别是:(1)长期慢性乙醇摄入后成熟和衰老大鼠小脑突触损失的特征;(2)乙醇戒断在大鼠器官型海马培养物中既引起神经毒性又抑制神经元恢复过程;(3)暴饮引起的脑损伤:遗传和年龄相关影响;(4)暴饮乙醇引起的脑损伤:水肿、花生四烯酸和组织坏死因子α(TNFα)的作用;(5)环磷酸腺苷级联反应、干细胞与乙醇。综合这些研究表明,酒精性神经变性在中毒和戒断期间通过多种机制在多个脑区发生。